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We previously identified a MOZ-TIF2 (transcriptional intermediary factor 2) fusion gene from a young female patient with acute myeloid leukemia (AML) (Liang et al., 1998). MOZ related chromosome translocations include MOZ-CREB-binding protein (MOZ-CBP, t(8;16)(p11;p13)), MOZ-P300(t(8;22)(p11;q13)), MOZ-TIF2(inv(8)(p11q13), and MOZNCOA3(t(8;20)(p11;q13)) (Esteyries et al., 2008; Troke et al., 2006). In an animal model, the MOZ-TIF2 fusion product successfully induced the occurrence of AML (Deguchi et al., 2003). Though the mechanisms for leukemogenesis of this fusion protein are poorly understood, analysis of functional domains in the MOZ-TIF2 fusion protein discloses at least two distinct functional domains: 1) the MYST domain containing the C2HC nucleosome recognition motif and the histone acetyltransferase motif in the MOZ portion and 2) the CID domain containing two CBP binding motifs in the TIF2 portion. Together these domains were responsible for AML in mice caused by injecting bone marrow cells transduced with retrovirus containing the MOZ-TIF2 fusion gene. Furthermore, MOZ-TIF2 conferred the properties of leukemic stem cells (Huntly et al., 2004). The MOZ-TIF2 transduced mouse common myeloid progenitors and granulocyte-monocyte progenitors exhibited the ability to serially replated in vitro. The cell line derived from transduced progenitors could induce AML in mice. Interestingly, the C543G mutation in C2HC nucleosome recognition motif or in the CBP binding motif (LXXLL) blocked the self-renewal function of MOZ-TIF2 transduced progenitors. More recently, a study using PU.1 deficient mice demonstrated that the interaction between MOZ-TIF2 and PU.1 promoted the expression of macrophage colony–stimulating factor receptor (CSF1R). Cells with high expression of CSF1R are potential leukemia initiating cells(Aikawa et al., 2010). Models suggesting that aberrant transcription by the interaction between MOZ fusion proteins and transcription factors, AML1, p53, PU1, or NF-kB have been well reviewed(Katsumoto et al., 2008).

MOZ-TIF2 Fusion Protein Binds to Histone Chaperon Proteins CAF-1A and ASF1B Through Its MOZ Portion